SBML generated from Reactome version 72 on 6/7/20 6:30 AM using JSBML version 1.3.1.

In the presence of Netrin1, DCC and UNC5 generate attractive and repulsive signals to growing axons. In the absence of Netrin-1, DCC induces cell death signaling initiated via caspase cleavage of DCC and the interaction of caspase-9. Recent reports have shown that UNC5 receptors similarly induce apoptosis in the absence of Netrin-1. These reactions proceed without a requirement for cytochrome c release from mitochondria or interaction with apoptotic protease activating factor 1 (APAF1). DCC thus regulates an apoptosome-independent pathway for caspase activation. DCC and UNC-5 are hence defined as dependence receptors. Dependence receptors exhibit dual functions depending on the availability of ligand. They create cellular states of dependence on their respective ligands by either inducing apoptosis when unoccupied by the ligand, or inhibiting apoptosis in the presence of the ligand.

GarapatiPhani Vijay

GarapatiPhani Vijay

CookJustinOICR

2009-04-27T13:36:03Z2020-03-10T23:32:12Z2008-07-16T18:42:16Z

Derived from a Reactome EntityWithAccessionedSequence. This is a protein

Derived from a Reactome EntityWithAccessionedSequence. This is a protein

Derived from a Reactome Complex. Here is Reactomes nested structure for this complex: (Q9Y5V3, Q6ZN44). Reactome uses a nested structure for complexes, which cannot be fully represented in SBML Level 3 Version 1 core

The neurotrophin receptor-interacting melanoma-associated antigen (MAGE) homologue, NRAGE, known to be a regulator of apoptosis, has been identified as a specific binding partner of UNC5H1. NRAGE utilizes two mechanisms to induce UNC5H1mediated apoptosis in cells: first, through the degradation of the caspase inhibitor X-chromosome-linked inhibitor of apoptosis protein (XIAP), and second, through the activation of the proapoptotic c-JUN N-terminal kinase (JNK) signaling pathway.